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Vascular Endothelial Dysfunction with Aging in Healthy Adults is Related to Total White Blood Cell Count and Selective Immune Cell Populations
Author(s) -
Seibert Sara Marian,
Donato Anthony J.,
Lawson Brooke R.,
Seals Douglas R.,
Walker Ashley E.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.967.13
Subject(s) - sodium nitroprusside , medicine , white blood cell , endothelial dysfunction , endothelium , endocrinology , vasodilation , immune system , immunology , nitric oxide
Vascular endothelial dysfunction (VED) develops with aging and contributes to increased risk of cardiovascular (CV) diseases. White blood cell count (WBC) is an independent predictor of CV events in middle‐aged and older adults (MA/O), but its relation to age‐associated VED is unknown. In 27 healthy adults free of infections (18–72 y), WBC was inversely related (r=−0.47, P<0.05) to endothelium‐dependent dilation (EDD), but was not related (P>0.05) to endothelium‐independent dilation (maximal forearm blood flow responses to acetylcholine and sodium nitroprusside, respectively). EDD was 41% lower (9.3±1.4 vs. 15.8±2.4 mL tissue −1 min −1 , mean±SE, P<0.05) in MA/O with higher WBC (6.0±0.2 10 9 /L, range 5.0–7.1, 65±1y, n=9/5m) than MA/O with lower WBC (4.0±0.2 10 9 /L, 3.4–4.8, 63±1y, n=9/6m) despite no differences in CV risk factors. EDD was similar in the MA/O with lower WBC vs. young controls with higher mean WBC (16.2±2.5 mL tissue −1 min −1 ; WBC 4.9±0.6 10 9 /L, range 3.0–8.9, 22±2y, n=9/7m,). EDD also was inversely related to WBC differential counts for neutrophils (r=−0.56, P<0.01), monocytes (r=− 0.34, P<0.05), eosinophils (r=−0.46, P<0.01), and basophils (r=−0.36, P<0.05), but was not related to lymphocytes (P=0.38). These results indicate that VED with aging is related to greater total WBC and elevations in selective populations of circulating immune cells. NIH AG006537 , AG013038 , AG022241 , AG000279